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Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
Review of the Physiology of Acid-Base Balance
Acid-Base Disorders
Concept of the Anion Gap
Interpreting the ABG and Clinical Applications
Exercises
F. Three-phased series mechanism that responds to the initial change
from normal acid-base status
1. Buffering – most rapid chemical process (in onset); this
refers to the ability of a solution containing a weak or poorly
dissociated acid and its anion to resist a change in pH upon
addition of a strong acid;
 this means that when an acid is introduced, it is immediately
buffered, resisting a change in pH
* acid still remains (compared with acids undergoing #2
mechanism: compensation)
ex. protein – albumin
REVIEW OF THE PHYSIOLOGY OF
ACID-BASE BALANCE
A. Definitions
Acid = H+ donor
Base = H+ acceptor
Acid
(H+ donor)
H2CO2
H3PO4
H2PO4-
Base
(H+ acceptor)
HCO3H2PO4HPO4=
Major Buffers:
HHb
H2PO4
H2CO3
The definition of base/acid does not depend on the charge. Note that
H2PO4- can be both an acid and a base.
 Definition is based on ability to donate/accept H+
B. Acid Strength
The strength of an acid depends on its solubility.

Strong acid – one which, when in solution, is completely or
almost completely dissociated; very little exist as
undissociated
HA  H+ + A
Weak acid – one which when in a solution is only slightly
dissociated; important in biological systems - type used in
our body; dissociation is reversible; can exert a positive or
negative effect of H+ ion to/from solution
HA  H+ + A-
H+ + HbH+ + HPO=
H+ + HCO3-
[From 2011]
The Respiratory Buffer Response
A normal by-product of cellular metabolism is carbon dioxide (CO2).
CO2 is carried in the blood to the lungs, where excess CO2 combines
with water (H2O) to form carbonic acid (H2CO3). The blood pH will
change according to the level of carbonic acid present. This triggers the
lungs to either increase or decrease the rate and depth of ventilation
until the
appropriate amount of CO2 has been re-established. Activation of the
lungs to compensate for an imbalance starts to occur within 1 to 3
minutes.
Other examples of buffers include :
a.
pCO2/HCO3- (independently regulated by the
lungs and kidneys)
b.
Hemoglobin buffer system: When in the deoxy
form, hemoglobin can buffer more acid. Co2 is
transported to the lungs as HCO3c.
Cellular and plasma proteins, intracellular organic
phosphates, bone (carbonates and phosphates)
D. Sources of Hydrogen Ion Loss
*pH maintained at a very, very narrow range
1. Loss of H+ in the vomitus: gastric secretions
2. Loss of H+ in the urine
 The only two pathways by which a person can lose H+
2.
Compensation - a process of slower onset than buffering but
much more effective in returning pH toward normal.
* because you remove a certain acid/base (compared with
those in #1 mechanism: buffering)
E. Threats to pH
1. Volatile acids: CO2
CO2: major end product in the oxidation of carbohydrates. Fats and
amino acids can be regarded as an acid by virtue of its ability to react
with water to form carbonic acid (H2CO3) which can dissociate to form
H+ and HCO3-.
2.



The Renal Buffer Response
In an effort to maintain the pH of the blood within its normal range, the
kidneys excrete or retain bicarbonate (HCO3
-). As the blood pH decreases, the kidneys will compensate by retaining
HCO3- and as the pH rises, the kidneys excrete HCO3- through the
urine. Although the kidneys provide an excellent means of regulating
acid-base balance, the system may take from hours to days to correct
the imbalance. When the respiratory and renal systems are working
together, they are able to keep the blood pH balanced by maintaining 1
part acid to 20 parts base.
C. Sources of Hydrogen Ion Gain = Bicarbonate loss
1. Generation of H+ from CO2
2. Production of acids from metabolism of protein and other
organinc molecules
3. Gain of H+ because of loss of HCO3- in diarrhea or other
nongastric fluids
4.
Gain of H+ because of loss HCO3 in the urine
 Gaining an acid is equivalent to losing a base. Or losing an acid is
equivalent to gaining a base. Yep.
CO2 + H2O  H2CO3 
carbonic acid
1
a. Hypotension: decreased BP : increased lactic acid in
hypoxic cells (glycolysis shifts to lactic acid production in hypoxic states
versus shift to Kreb’s cycle in normal oxygen states)
b. DKA: decreased insulin: increased production of ketoacids.
OUTLINE
I.
II.
III.
IV.
V.
EXAM
-
H+ + HCO3-
Fixed acids: Sulfuric and Phosphoric Acids; usual exogenous
sources are meaty foods / proteins. Thus, a meat eater
would produce acids more, while a vegetarian would
produce alkali more.
Organic Acids: Lactic acid (muscle fatigue/anaerobic metabolism);
acetoacetic acid and beta-OH butyric acid (starvation, DM – absence
of insulin) formed during the metabolism of carbohydrates and fats
Usually seen in pathologic states
In the physiological state, organic acids are present in small
amounts because they are readily metabolized by the liver into
bicarbonates. Accumulation of organic acids is evident in pathological
states. (e.g. lactic acid is generated in tissue ischemia)
-
The respiratory system, by altering PCO2 constitutes
compensation in metabolic disorders. The lungs handle the
respiratory component by either blowing off or retaining
CO2.
The kidneys by altering plasma [HCO2-] provide
compensation in respiratory disorders. The kidneys handle
the metabolic component in terms of removing or retaining
HCO3.
Respiratory compensation is faster (3 – 4 hrs) than renal
compensation (42 – 48 hrs delayed), but renal
compensation is more complete.
*acute if not compensated yet
2012: The kidneys and lungs are the yin-yang stuff of the body. The
kidneys handle the metabolic component in terms of removing or
retaining HCO3. The lungs, on the other hand, handle the respiratory
component by either blowing off or retaining CO2. Both work to
maintain body pH in the face of fluctuating CO2/HCO3 values.
Page 1 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
 Again, when an acid is introduced, the buffer system will try to bring
pH back to normal (it will never normalize, though). If the pH remains
neutral after adding acid, then acidic/alkali problems exist.
3.
Correction - the definitive process that returns all the acidbase variables to normal.
ex. kidney failure – recovery; kung problems – recovery
G. The Law of Mass Action and the Henderson-Hasselbach Equation
HA
H+ + Av1 = k1 [HA]
v2 = k2 [H+] [A-]
1
All gases partially dissolve/dissociate in water. The degree to which this
occurs is proportional to the partial pressure of gases in solution. In
humans, the partial pressure of CO2 is 40mmHg.
[CO2] dis
= α P CO2
= 0.03mmol/L/mmHg x 40 mmHg
= 1.2 mmol/L
where 0.03 mmol/L/mmHg is the solubility constant for CO2 in the
plasma at normal temperature (therefore, febrile/hypothermic states
may affect the solubility constant).
BASIC RULE: in body fluid, at equilibrium:
v1 = v2
since they’re equal, substituting for v1 and v2:
k1 [HA] = k2 [H+] [A-]
EXAM
 Equilibrium
In plasma at 37o C, K’a = 800 nanomol/L
and [ CO2 ] dis = 0.03 x P CO2
Thus:
[ H+ ] = (800x0.03) P CO2
[HCO3- ]
[ H+ ] = 24 P CO2
[HCO3- ]
If k1/k2 = ka, then:
ka [HA] = [H+] [A-]\
Solving for [H+]:
* In most ABG machines, pCO2 is directly measured; [HCO3-] is
only measured via an equation
[H+] = ka [ HA ]
[ A- ]
This is the Henderson equation.
***To keep the concentration of H+ constant: if there is an
increase in acid concentration [HA], the base concentration [A-]
should increase, too.
If you want to measure the pH:
Taking the -logarithm of both sides:
-log [H+] = - log ka - log [HA]/[A-]
Since the normal H+ concentration is 40 nanomol/L and the P CO2 is
40 mmHg, the normal [HCO3- ] can be calculated:
At pH of 7.4,
40 = 24 x
40
.
[HCO3- ]
[ HCO3-] = 24 mmol/L
The normal free [H+] is very minimal, 40 nmoles/L only. This
ion is very reactive and can easily displace other cations in enzymatic
reactions.
By comparison, Sodium (Na) is around 135-145 mmol/L!
if: pH = - log [H+], pka = - log ka
and + log [A-] / [HA] for - log [HA] / [A-]
then:
pH = pka + log [ A- ]
[ HA ]
Must Know!
This is the Hasselbach equation.
***However, it is difficult to get acid-base relationship using this
equation.
H. HCO3/CO2 Buffer system
CO2(g)  CO2 (aq) + H20  H2CO3 H+ + HCO3
removed
 Since H2CO3 readily dissociates to H+ and HCO3, we can say
that CO2 + H2O goes straight to it (minimal amounts of H2CO3).
The equation can be simplified to:
[CO2 ] dis + H2O  H+ + HCO3-
Normal values:
[HCO3] = 24 mmol/L
pCO2 = 40 mmHg
[H+]
= 40 nanomole/L
Plasma pH = 7.4
[ H+ ] = 24 pCO2
[HCO3- ]
I. Isohydric Principles
From the law of mass action, the acid/base ratio of any weak
acid is determined by its Ka and the H+ concentration of the solution.
Since the H+ concentration affects each buffer, the following
relationship is present:
[ H+ ] = Ka1 0.03 PCO2 = Ka2 [ H2PO4- ]
[HCO3- ]
[ HPO4= ]
= Ka3 [ HA]
[A-]
If the H+ concentration is altered, the acid/base ratios
of all the buffers in the solution are affected.
*can use any body buffer system
The law of mass action for this reaction is:
Ka = [ H+ ] [HCO3- ]
[CO2 ] dis [ H2O ]
Since the concentration of water is constant,
( Ka x [ H2O ]) can be replaced by:
Hasselbach equation:
pH = pka + log [A-] or pH = pka + log base
[HA]
acid
K’a = [ H+ ] [HCO3- ]
[CO2 ] dis
Note: K’a is equal to (Ka x [H2O]), so if you substitute it with the
previous equation, (the one with Ka), and you solve for K’a, you get
this equation.
Solving for [H+],
[ H+ ] = K’a [ CO2 ]
[ HCO3- ]
Note: It will make life easier if you can memorize this equation :-?
Since CO2 metab is in the lungs and HCO3 is in the kidneys:
pH = pKa + log kidneys - base
lungs - acid
 Note that the numerator in the above equation is the acid 
handled by the lungs, and the denominator is the base  handled by
the kidneys
Page 2 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
J. Relationship of pH to H+ concentration
Acidification: pH < 7.4
Alkalinization: pH > 7.4
(Acidemia)
(Alkalemia)
EXAM
ACID-BASE DISORDERS
K+ in Metabolic Acidosis
(nM)
H+
H+ doubles for each;
0.3 unit fall in pH
H+ halves for each
0.3 unit rise in pH
Organic
anions
H+
K+
K+
K+
SO4PO4=
A pH increase of just 0.3 decreases H+ to half the normal value, while
a pH decrease of just 0.3 doubles it!
 Normal pH is 7.4
Organic
acidosis
ex. H+  pH   7.1  free H+ is 80nM
Inorganic Acidosis
- eg. intentional ingestion of acids i.e. sulfuric acid, renal failure
 accumulation of sulfates & phosphates
- when H+ increases, it moves into the cell while inorganic anions (ie
PO4, SO4) stay out, so K+ goes out to maintain balance, thus there
would be an increase in serum concentration of K+.
* inorganic acidosis  extreme K+ depletion compared to
organic acidosis
MUST KNOW! MUST UNDERSTAND!
What is the H+ if the plasma pH is 7.16?
pH
H+
7.4
40
7.16
x
.24
y
.3
.3
_____
-40
= _____
.24
y
-40
TABLE 1. CHARACTERISTICS OF PRIMARY ACID – BASE DISTURBANCES
1º
Disorder
pH
[H+]
Compensation
Disturbance
Metabolic
↓
↑
↓ PaCO2
↓ [HCO3-] -oracidosis
↑ PaCO2
Metabolic
↑
↓
↑ [HCO3-] -or↑ PaCO2
alkalosis
↓ PaCO2
Respiratory
↓
↑
↑ PaCO2 -or↑ [HCO3-]
Acidosis
↓ [HCO3-]
Respiratory
↑
↓
↓ PaCO2 -or↓ [HCO3-]
alkalosis
↑ [HCO3-]
* Metabolic  HCO3Respiratory  pCO2

Problems in handling of HCO3- is a metabolic problem

Problems in handling CO2 means that there is a respiratory
problem

Compensatory response goes in the same direction as the 1o
disturbance parameter in bold
 How to look at it: a decrease in pH means there is retention of acid or
a loss of a base.
Acidosis = decrease in pH due to accumulation of H+
80
40 – x = y
40 + 32 = x
X = 72
y = -32
Step 1:
Step 2:
Step 3:
Step 4:
Step 5:
Step 6:
Inorganic
acidosis
Organic Acidosis
- eg. lactic acidosis, ketoacidosis
- as H+ increases, it moves into the cell together with organic
anions, thus there is no change in serum concentration of K+.
Exercise:
What is the H+ if the plasma is 7.16?
pH
H+
7.4
40
7.16
x
7.10
80
7.10
1
normal pH minus lowest
7.4 – 7.10 = 0.3
normal H+ minus lowest
40 – 80 = -40
normal pH minus x
7.4 – 7.16 = 0.24
normal H+ minus x = y
40 – x = y
divide the answer in step 3 by 0.3 units
0.3/0.24 = -40/y
y = -32
substitute y in equation in step 4
40-x = y
40+32 = x
x =72
↓ HCO3- or ↑ PaCO2
 Note: This only works for computing values near physiologic pH,
1º Disturbance:
Compensatory:
since at that range, the curve of values is relatively linear.
Application:
pH = 7.6
H+ = 26nmol/L
pCO2 = 26mmHg
HCO3- = ?
metabolic
↓ PaCO2
respiratory
↑ HCO3-
To recognize the primary problem, look at the:
1. pH
2. PaCO2 then [HCO3-]
TABLE 2. COMPENSATORY RESPONSES IN SIMPLE ACID-BASE DISORDERS
H+ = 24 x pCO2/HCO3(recall encircled equation in the previous page)
* Ex. salicylic acid poisoning  H+
Tx: alkalinize urine  pH=7.5
Disorder
How much HCO3- should be given?
26 = 24 x 26/HCO3HCO3- = 24
 24 should be considered normal, BUT pH is abnormal (7.6), so
another parameter must be abnormal, too. (remember the Must Know!
box in page 2?)
Metabolic
acidosis
Metabolic
alkalosis
Respiratory
Acidosis
Respiratory
alkalosis
1 Abnormality
HCO-
2 Response
Loss of
3 or
gain of H+
Gain of HCO-3 or
loss of H+
Hypo-ventilation
↑ ventilation
HCO3- generation
Hyper-ventilation
HCO3- consumption
↓ ventilation
Page 3 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas

TABLE 3. RENAL AND RESPIRATORY COMPENSATION TO 1 ACID – BASE
DISTURBANCES
Compensatory
Disorder
1 Abnormality
Response
Metabolic
↓[HCO3-] -or1.2mmHg DECrease in PaCO2 for every
acidosis
↑PaCO2
1mEq/L fall in HCO-3
Metabolic
↑[HCO3-] -or0.7mmHg INCrease in PaCO2 for every
alkalosis
↓PaCO2
1mEq/L rise in HCO3Respiratory
Acidosis (acute)
↑PaCO2 -or1mEq/L INCrease in [HCO-3] for every
Ex. pneumonia,
↓[HCO3-]
10mmHg rise in PaCO2
PaCO2 = 15

Answer:
Given the ff. ABG results, describe the acid-base status and adequacy
of compensation:
Ex 1.
[HCO3-] = 24
PaCO2 = 40
pH = 7.40
PaCO2 = 22

Normal pH; Low [HCO3-]; Low PaCO2.
To determine the dominant factor (whether it is
metabolic acidosis or respiratory alkalosis) in the
maintenance of such pH, compute how deviated each
value is from the normal.
Since there is no greater parameter (the deviations are equal), the acid
base status is a…
COMBINED METABOLIC ACIDOSIS & RESPIRATORY ALKALOSIS.
Arterial Measurements in Hypothetical Acid-Base Disorder
[HCO3-]
PCO2
meq/L
mmHg
pH = 7.24

Answer:
a. Low pH; Low [HCO3-]; Low PaCO2
PURELY METABOLIC ACIDOSIS
b. Ideal compensatory response: remember that in metabolic
acidosis, there is a 1.2mmHg decrease in PaCO2 for every 1mEq/L
fall in HCO3-. Thus:

Fall in HCO3- = normal value (NV) – given value
= 24 – 9
= 15

(N)
[HCO3-] = 24 (normal)
PaCO2 = 40 (normal)
= 9 (patient) Deviation
= 15 (patient)
= (24-9)/24
Deviation = (40-15)/40
= 0.625
= 0.625
 determine which parameter has a greater change in value of
deviaion
Answer: NORMAL
 Therefore, REMEMBER THESE VALUES!
Ex 2.
[HCO3-] = 9

pH = 7.40



1
Clinical situation that can present with this scenario:
renal failure with hyperventilation (as an early
compensatory
response),
proceeding
to
hypoventilation, after fatigue sets in.
Ex 4.
[HCO3-] = 9
acute asthma
Respiratory
Alkalosis
↓PaCO2 -or2mEq/L DECrease in [HCO-3] for every
(acute)
↑[HCO3-]
10mmHg fall in PaCO2
 In metabolic processes, the key value to remember is 1 mEq/L
change. In respiratory processes, the key value is 10mmHg change.
* Chronic respiratory conditions – ex. COPD, restrictive lung dses
EXAM
pH
Acid base status
24
40
7.40
Normal
9
22
7.23
Pure metabolic acidosis
9
40
6.98
Primary metabolic and
secondary
respiratory acidosis
9
15
7.40
Combined metabolic acidosis
and respiratory alkalosis
Compensatory response (CR) = 15 x 1.2 (refer to table
3)
= 18mmHg
CONCEPT OF THE ANION GAP

Ideal compensation = NV – CR
= 40 – 18
= 22mmHg  2  20–24

Since actual PaCO2 (22 mmHg) is within the ideal PaCO2
(20–24 mmHg).
Note:  2 in ideal compensation either for HCO3 or pCO2
 ADEQUATE Compensation
*PURE METABOLIC ACIDOSIS
– pure siya if maximum pCO2 value is within 20-24 mmHg. If
> 24mmHg, there is now a 2o respiratory acidosis.
 Total cations and anions in the ECF should be equal.
 Anion gap refers to the anions not routinely measured on serum
electrolytes.
 The dominant anions are Sodium (140 mmol/L) and Chloride (105
mmol/L)
 Usually negatively charged proteins, SO4-, PO4 Generally, Na+ is the only cation considered in computing the
anionic gap (since others have relatively small concentrations in
serum).
 Any minor increase in K, Ca and Mg can be fatal!
K+
Ca++
Mg++
*ex. PaCO2 = 25mmHg  1o Metabolic Acidosis with 2o
Respiratory Acidosis
Pr- ex. albumin; SO4=; PO4=
Gets? Kamusta? If malabo, review muna previous pages…
Ex 3.
[HCO3-] = 9
PaCO2 = 40

Answer:
AG
HCO3-
(N)
pH = 6.98

Na+




Low pH; Low [HCO3-]; Normal PaCO2.
1 METABOLIC ACIDOSIS, 2 RESPIRATORY ACIDOSIS
Since there is a decrease in [HCO3-], there should have
been a corresponding PaCO2 decrease.
But since PaCO2 is normal, it means no compensation
occurred!
If it rises above 40, then it’s time to intubate the
patient.
Cl(major
anion)
*K (4), Ca (2.5), Mg (0.8 -1)– very narrow range
*Pr, SO4, PO4 – not routinely measured in lab
Page 4 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
 Anion gap is therefore defined as the DIFFERENCE between the
EXAM
1
INTERPRETING THE ABG AND
CLINICAL APPLICATIONS
concentrations of measured cations and measured anions (since
laboratory tests can’t measure it directly)
1.
AG = [Na+] – ( [Cl-] + [HCO3-] )
Normal Value = 12  2
2.
3.
4.
5.
ANION GAP Illustrations
6.
Get a good History and PE. (it could tell you (1) the need
for blood gas assessment and if there’s an acid-base
disturbance and (2) what to expect in the interpretation
ex. Renal failure  high anion gap)
Get your ABG.
Determine the serum electrolytes at the same time.
Know the primary disorder.
Compute for the range of compensation. Don’t forget to
2!
For METABOLIC ACIDOSIS: GET THE ANION GAP
1. FOR HIGH ANION GAP METABOLIC ACIDOSIS:
Get ∆AG and compare it to ∆HCO3- to determine if there are other
HIDDEN METABOLIC PROBLEMS.
AG = AG – 12 (normal value)
∆HCO3- = 24 (normal value) - [HCO3]
Table 4. Determining Hidden Problems in High Anion Gap Metabolic
Acidosis
∆AG = ∆HCO3Pure High 10 lactate (lactic acid)
AG
H+ + lactate): H+ (buffered) + HCO3 
metabolic
CO2 + lactate goes to AG  increasing
acidosis
A. Normal ion distribution
B. High anion gap metabolic acidosis (accumulation of
anions)




Lactic acidosis: lactate
Ketoacidosis: B-hydroxybutyric acid
Renal failure: sulfate, phosphate, urate
Ingestions
- salicylates: ketones, lactatem salicylate
- methanol/ formaldehyde
- ethylene glycol: glycolate/ oxalate
AG so high AG
∆AG > ∆HCO3-
*ex. Adding lactic acid (H+ + lactate): H+ (buffered) + HCO3  CO2 +
lactate goes to AG  increasing AG

-
- diarrhea
Renal HCO3- loss
- types 1 Renal Tubular Acidosis (RTA)
- Type 2 RTA
- hyperkalemia
Ingestion:
ammonium chloride (NH4Cl)
High
AG
metabolic
acidosis w/
normal
metabolic
acidosis
Renal failure + diarrhea
(Kaw naman try mo explain?)
Table 5. Determining Hidden Problems in Normal Anion Gap
Metabolic Acidosis
∆Cl- = ∆HCO3-
Metabolic Acidosis and the Anion Gap
Na+ X-
Pure
Normal
metabolic acidosis
AG
Na+ HCO3-
H2CO2
H2O + CO2
Normal
Normal
AG Acidosis
140
105
24
11
High
AG Acidosis
140
105
14
21
1
∆Cl- < ∆HCO3-
+10
11
0
Ingestion of poisons
+ NGT
HCO3= 20: dapat 14
lang (from 24-10) so
may na-add na 6 HCO3
so may met alka
-10
0
1
Normal AG metabolic
acidosis with metabolic
alkalosis
10 HCl  H+ (met acid)
and  Cl by 10, do not
add in AG so ((N) AG)
140
115
14
11
-10
Diarrhea + ingestion
of poisons
10 HCl  H+ and 
HCO3 by 10 (met acid),
 Cl, do not add in AG so
((N) AG)
∆Cl- > ∆HCO3-
Na+
ClHCO3AG
Δ HCO3Δ AG
LactΔ Lact
Renal failure (accumulation of anions) 
adding to acidity and anions go to AG so
increasing AG more  high AG met acid
2. FOR NORMAL ANION GAP METABOLIC ACIDOSIS:
Get ∆Cl- and compare it to ∆HCO3- to determine if there are other
hidden metabolic problems (compare them since they are the only
parameters that change, when AG is normal).
*ex. add’n of HCl (H+ + Cl-): H+ (buffered) + HCO3  H2CO3  CO2 +
H2O + Cl- (Cl does not go to AG so Normal pa din AG)
H+ X-
Renal failure +vomiting
Vomiting   H-  met alka
∆AG < ∆HCO3-
C. Normal anion gap metabolic acidosis

Gastrointestinal loss of HCO3
High
AG
metabolic
acidosis w/
metabolic
alkalosis
+10
Normal AG metabolic
acidosis with high AG
metabolic acidosis
2013 B: Another process
which
consumes
bicarbonate>> metabolism
Ingestion of poisons
+ renal failure
10 HCl  H+ (met acid)
and  Cl by 10, do not
add in AG so ((N) AG)
HCO3 = 4: dapat 14
(from 24-10) so may
naconsume na 10 HCO3
or may naaadd na acid
Page 5 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
i.e lactic acid, ketoacid
so may high AG met
acid
EXAM
1
1. What are the diagnostic clues for the presence of a possible blood gas
abnormality?
- The patient is from a place of high altitude (The Andes) 
compensatory  in HCO3
- we need to get pH, PCO2 values
POP Quiz!
HPE
Vomiting
NGT
Comatose not intubated
Comatose intubated
Renal failure + diarrhea
Possible Interpretation
Metabolic alkalosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
High AG metabolic acidosis with
Normal metabolic acidosis
High AG metabolic acidosis with
hidden metabolic alkalosis
Renal failure + vomiting
*If px gains H+, it may also mean that px gains HCO3.
Not discussed but included in the ppt:
BUFFERS
1.
pCO2/HCO3- (independently regulated by the lungs and kidneys)
2.
Hemoglobin buffer system: When in the deoxy form, hemoglobin can buffer more acid.
CO2 is transported to the lungs as HCO33.
Cellular and plasma proteins, intracellular organic phosphates,
bone (carbonates and phosphates)
The Hemoglobin Buffer System:
9
6 ClHCO3KCl
Cl6
K+
HCO3-
HHb
Hb-
HHb
7
O2
HHbO2
KHCO3
K+ 5
HCO3-
4
H+
8
Justin: Hi
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A, renal
na!!! we
can do this!
Hi to paul,
motch,
rommel!
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CO2
CO2
CELL
KHCO3
10
H2CO3
CO2
CA
1
11
H2 O
Lab works:
pH = 7.11

pCO2 = 25.4 
HCO3- = 7.8 
Na+ = 141 mmol/L
K+ = 2.4 mmol/L
Cl- = 111 mmol/L
Crea = 250mmol/L
2. What is your primary disorder?
- low pH and decreased HCO3  Metabolic acidosis
12
2
CO2
PLASMA
Problem 2:
A 36-year old woman has been having watery diarrhea for the past 3
days after eating pork barbeque. When she was brought to emergency
room, she was noted to be weak-looking with sunken eyeballs and
poor skin turgor.
Vital signs: BP = 90/60mmHg HR = 120/min RR = 26/min
CA
H2 O
3
HCO3-
KHCO3
KHbO2
H2CO3
JF: Hi
everyone!
Congrats sa
mga nanalo
sa Culture
Week!!!
Ang galling
ng 2013!!!
HCO3Cl-
K+
- HCO3 value can be a 1o or a 2o problem
1. What are your diagnostic clues?
- watery diarrhea (she is losing bicarbonates)  (N) AG metabolic
acidosis)
- weak-looking, sunken eyeballs, poor skin turgor  dehydration  
perfusion  renal failure  high AG met acid
- tachycardic  worsening acidosis
- weak-looking, hypotensive  maybe lactic acidosis  renal failure 
high AG metabolic acidosis
Cl-
KCl
2. What is your interpretation of the serum HCO3-?
- Strictly speaking, the serum HCO3- is below normal (N=24nmol/L), but
since we have to take into account the place of origin of the patient
(The Andes), the serum HCO3- is actually just right for her to function
well.
CO2
3. What is your compensatory response?
ALVEOLAR CAPILLARY
Venous blood gas
Fall in bicarbonate:
Expected fall in PCO2:
Expected PCO2 level:
24 - 7.8 = 16.2
16.2 x 1.2 = 19.44
40 - 19.44 = 20.56  2
= 18.56-22.56
Given pCO2: 25.4 ( > the upper limit of range or > 22.56)
 Not compensated
 2o (mild) Respiratory acidosis
Arterial blood gas
So why worry about acids and bases?
pH = 7.8 incompatible with life
pH = 7.7 seizures, tetany
pH = 7.6 muscle cramps, fatigued, irregular
heart beat
pH = 7.5 breathing is slow
Worsening
Alkalosis
4. What is the anion gap?
AG = [Na+] – ( [Cl-] + [HCO3-]
=141 – (111+ 7.8) = 22.2
22.2 > 12  2 (10-14)
 High anion gap metabolic acidosis
pH = 7.4 normal arterial pH
pH = 7.3 breathing is rapid
pH = 7.2 fatigued, nausea and abdominal pain,
pulse and breathing rapid
pH = 7.1 blood pressure falling due to
decreased force of heart beat and vasodilation,
irregular pulse
pH = 7.0 decreased consciousness
pH = 6.8 incompatible with life
Worsening
Acidosis
5. Is there a hidden problem?
Since it is a HIGH AG metabolic Acidosis,
Compare Δ AG __?____ Δ HCO322 - 12 _______ 24 - 7.8
10 ___<____
16.2
(8-12)
(16.2 > 8-12) – may naconsume na at
least 4.2 addtl HCO3 or may naadd na acid
 Yes, a Normal anion gap metabolic acidosis
EXERCISES
Before starting with the exercises,
Let us review
*sabi ni ma’am, easier daw na tingnan na lang yung difference between
AG & HCO3 ex. in this case, 16.2-10 = 6.2. If ≥ 2, it is significant. There is
a hidden problem. If Δ AG < Δ HCO3, there is metabolic acidosis. If Δ AG
> Δ HCO3,there is metabolic alkalosis.
PaCO2 = 40 mmHg
[H+]
= 40 nmol/L at pH = 7.4  2 for our purposes
[HCO-3] = 24 nmol/L
6. What is your final interpretation?
*If you’re not interested in getting pO2, you can use venous blood gas
Also, just follow these steps in solving
value.
for the problems ahead.
Problem 1
Step1: pH (Is it a problem of acidosis or alkalosis?)
A 21 year old Andean woman had no medical problems. She was
Step 2: PaCO2 (Is it respiratory?)
accepted as a first year medical student in the USA. Before leaving, she
Step 3: [HCO3-] (Is it metabolic?)
underwent a complete history and physical examination, including
Step 4: Check for compensatory response (Tables 2&3, p. 4 )
blood tests. Everything was normal except for a serum HCO3- of 15
Step 5: Compute for anion gap (In metabolic acidosis cases)
mmol/L.
AG = [Na+] – ( [Cl-] + [HCO3-] )
Normal Value = 12  2
HIGH ANION GAP METABOLIC ACIDOSIS WITH 2o RESPIRATORY
ACIDOSIS AND A HIDDEN NORMAL ANION GAP METABOLIC ACIDOSIS
Problem 3:
A 27 year-old male with insulin-dependent diabetes mellitus has not
been taking his insulin and is admitted to the hospital in a
semicomatose condition. The following laboratory data are obtained:
Page 6 of 8
MONDAY
March
2010
Step| 6:
Check if1,there
is a hidden problem (Tables 4&5, p.5-6)
*Usually (but not always: Hidden Problems are seen in High
AG metabolic acidosis
Step 7: State the final interpretation/diagnosis completely.
JF, Justin, Alex, Suzie
Dr. Montemayor
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
[ Na+] = 140 meq/L pH = 7.10

[ K+ ] = 7.0 meq/L pCO2
= 20 mmHg 
[ Cl-] = 105 meq/L
[ HCO3-] = 6 meq/L 
Glucose = 800 mg/L
1. What are your diagnostic clues?
- not been taking insulin for his DM  diabetic ketoacidosis  high AG
metabolic acidosis due to acetoacetic acid and/or beta-butyric acid
- semicomatose condition  fluid intake is most probably decreased 
respiratory acidosis
1
Since it is a HIGH AG metabolic Acidosis,
Compare Δ AG __?____ Δ HCO318.1 - 12 ___?____ 24 – 20.9
6.1 ____>____ 3.1
(4.1 – 8.1)
3.1< (4.1–8.1)**
**konti lang nagamit na HCO3. supposedly around 17.9 ang HCO3 but
20.9. Parang may nag-aadd ng HCO3…so look for other causes of
hypokalemia
 Metabolic alkalosis
2. What is your primary disorder?
Low pH, low HCO3  Metabolic Acidosis
6. What is your final diagnosis?
HIGH ANION GAP METABOLIC ACIDOSIS WITH METABOLIC ALKALOSIS
3. What is the compensatory response?
Fall in bicarbonate:
24 – 6 = 18;
Expected decrease in PCO2:
18 X 1.2 = 21.6;
Expected PCO2 level:
40 – 21.6 = 18.4  2
= 16.4-20.4
Given pCO2:
20 (within the expected level)
 Compensated
Problem 5:
A 45 y/o female with peptic ulcer disease complaining of persistent
vomiting. PE: 100/60 mmHg, poor skin turgor, flat neck veins.
[Na+] = 140 mEq/L
pH = 7.53

[Cl-] = 86 mEq/L
PaCO2 = 53 mmHg

[K+] = 2.2 mEq/L
[HCO3-] = 42 mEq/L 
1.
4. What is the anion gap?
AG = [Na+] – ( [Cl-] + [HCO3-] )
= 140 – (105 + 6) = 29 > 12  2 (10-14)
 High Anion gap metabolic acidosis
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EXAM
2. What is your primary disorder?
- high pH, high HCO3  Metabolic alkalosis
5. Is there a hidden problem?
Since it is a HIGH AG metabolic Acidosis,
Compare Δ AG __?____ Δ HCO329 - 12 _______ 24 - 6
17 ___<___
18
(15-19)
(18 is within 15-19)
 No hidden problem
3. What is your compensatory response?
Increase in bicarbonate:
42 – 24 = 18
Expected rise in pCO2:
18 x .7 = 12.6
Expected pCO2 level: 40 + 12.6 = 52.6  2
= 50.6 – 54.6
Given pCO2:
53 mmHg (within the expected range)
 Compensated
6. What is your final diagnosis?
HIGH ANION GAP METABOLIC ACIDOSIS, COMPENSATED
Problem 4:
A 17 year old male has a history of on and off weakness since 2 years
ago. A few hrs before admission, he can’t move his lower extremities.
[ Na+] = 154 meq/L pH
[ K+ ] = 2.3 meq/L pCO2
[ Cl-] = 115 meq/L
= 7.36

= 37.5 mmHg 
[ HCO3-] = 20.9 meq/L
Base excess = - 3.7
What are your diagnostic clues?
persistent vomiting  metabolic alkalosis
poor skin turgor  poorly perfused tissues  poorly
perfused kidneys  High AG metabolic acidosis

*Base excess = excess of a base (hehehe)
*If base excess is negative, there is an absence of an excess of the base.
Like in this case.
1. What are your diagnostic clues?
- on and off weakness  HPP or Hypokalemic Periodic Paralysis
- Severe hypokalemia  ms injury  toxic substance  acute renal
faillure
-DDx: (1) Rebal tubular acidosis  waste HCO3  (N) AG metabolic
acidosis
- (2) rhabdomyolysis  acute renal filure  High AG metabolic
acidosis
4. What is your final diagnosis?
 COMPENSATED METABOLIC ALKALOSIS
Not discussed:
Causes of Impaired HCO3- excretion that allow metabolic alkalosis to persist
 Decreased GFR
- Effective circulating volume depletion
- Renal failure ( usually associated with metabolic
acidosis)
 Increased Tubular Reabsorption
- Effective circulating volume depletion
- Chloride depletion
- Hypokalemia
- Hyperaldosteronism
Pathophysiology of Metabolic Alkalosis
1.
Why do patients become alkalotic?
2.
Why do they remain alkalotic, since renal excretion
of the excess HCO3- should rapidly restore normal
acid-base balance
Check serum and urine pH
2. What is your primary disorder?
Low pH, low HCO3  Normal Anion Gap Metabolic Acidosis
3. What is your compensatory response?
Decrease in bicarbonate:
24 – 20.9 = 3.1
Expected fall in PCO2 :
3.1 X 1.2 = 3.72
Expected pCO2 level:
40 – 3.72 = 36.27  2
= 34.27 – 38.27
Given pCO2:
37.5 mmHg (within expected range)
 Compensated
1.
Serum and urine pH both increased:
loss of acid through the GIT,
gain of alkali, exogenous
2.
Urine pH low:
loss of acid through the kidneys
(mineralocorticoid excess)
4. What is the anion gap?
AG = [Na+] – ( [Cl-] + [HCO3-] )
= 154 - (115 + 20.9)
= 18.1 > 12  2 (10-14)
 High anion gap metabolic acidosis
5. Is there a hidden problem?
Page 7 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
OS 214: Excretory System Module
Juan
Lecture 3: Interpretation of Arterial Blood Gas
PROXIMAL
PROXIMAL TUBULE
TUBULE REABSORPTION
REABSORPTION
Lumen
Proximal Tubule Cell
ISF
Na+
HCO3Na+
Na+
Na+
5
H+
H+
2
H+
H+
H2CO3
Na+
1
ATP
K+
H2CO3
CO2
4
H2O CA
CO2
1. Active transport of Na+
creates an intracellular (-)
allowing diffusion of Na+
2. H+ is secreted into the
lumen by the Na+ - H+
exchanger
3HCO3-
HCO3-
ATP
3
H2 O
Dr. Montemayor
3. H+ combines wth filtered
HCO3- to form H2CO3 and
then CO2 and H2O
4. CO2 diffuses into the cell
to combine with H2O to form
H2CO3 then H+ + HCO35. HCO3- returns to the
circulation by a Na+ - 3
HCO3- cotransporter
Problem 6:
A 54 year old lawyer complained of leg pains and eventually underwent
femoral popliteal bypass surgery. Preop renal function and acid-base
status were normal. 24 hours later, he was noted to be oliguric, cold
and clammy and drowsy. PE revealed a BP of 90/60 mm Hg.
HR = 126/min and absent pulses in his R foot.
EXAM
[ Na+] = 144 meq/L pH
= 7.36
[ K+ ] = 4.2 meq/L pCO2
= 54.0 mmHg
[ Cl-] = 105 meq/L
[ HCO3-] = 30.6 meq/L
1. What are your clinical clues?
2. What is the primary disorder?
3. Compensatory response?
4. Anion Gap?
5. Hidden problem?
6. Interpretation?
Problem 9:
A 25 year old patient with epilepsy suffered a grand mal seizure.
Immediately after the seizure, the ff labs were obtained:
[ Na+] = 140 meq/L pH
= 7.14
[ K+ ] = 4.2 meq/L pCO2
= 45.0 mmHg
[ Cl-] = 98 meq/L
[ HCO3-] = 14 meq/L
1. What are your clinical clues?
2. What is the primary disorder?
3. Compensatory response?
4. Anion Gap?
5. Hidden problem?
6. Interpretation?
[ Na+] = 140 meq/L pH
= 7.0

[ K+ ] = 6.4 meq/L pCO2
= 32 mmHg

[ Cl-] = 103 meq/L
[ HCO3-] = 8.0 meq/L

1. What are your diagnostic clues?
- oliguric, cold and clammy and drowsy  circulatory collapse, poorly
perfused kidneys  renal failure  high AG metabolic acidosis
- cold, clammy  poor tissue perfusion  lactic acidosis  High AG
metabolic acidosis
- (-) pulses in his ® foot  ischemia  lactic acidosis  high AG
metabolic acidosis
2. What is your primary disorder?
- low pH, low HCO3  Metabolic Acidosis
3. What is your compensatory response?
Decrease in bicarbonate:
24 – 8.0 = 16
Expected fall in PCO2 :
16 X 1.2 = 19.2
Expected pCO2 level:
40 – 19.2 = 20.8  2
= 18.8 – 22.8
Given pCO2:
32 mmHg > expected range
 Not Compensated  2O Respiratory Acidosis
4. What is the anion gap?
AG = [Na+] – ( [Cl-] + [HCO3-] )
= 140 - (103 – 8.0) = 29 > 12  2 (10-14)
 High anion gap metabolic acidosis
5. Is there a hidden problem?
Since it is a HIGH AG metabolic Acidosis,
Compare Δ AG __?____ Δ HCO329 - 12 ___?___ 24 – 8.0
17
___>___ 16
(15-19)
16 is within (15-19)
 No Hidden Problem
6. What is your final diagnosis?
HIGH ANION GAP METABOLIC ACIDOSIS WITH RESPIRATORY ACIDOSIS
Practice Problems:
Problem 7:
This is a 50 year old male who underwent nephrolithotomy for R
staghorm calculus. There was no ff-up after discharge. A few days
prior to admission, he complained of weakness, nausea and vomiting.
[ Na+] = 143 meq/L pH
= 7.25
K+ ] = 6.2 meq/L
pCO2
= 24.5 mmHg
[ Cl-] = 102 meq/L
[ HCO3-] = 10.8 meq/L
1. What are your clinical clues?
2. What is the primary disorder?
3. Compensatory response?
4. Anion Gap?
5. Hidden problem?
6. Interpretation?
Problem 8:
A 74 year old male was admitted for pneumonia.
He presented with the ff. labs.
Page 8 of 8
MONDAY | March 1, 2010
JF, Justin, Alex, Suzie
1